LXR ligands induce apoptosis of EGFR-TKI-resistant human lung cancer cells in vitro by inhibiting Akt-NF-κB activation

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are efficient in treating patients with non-small cell lung cancer (NSCLC) harboring EGFR activating mutations. Unfortunately, nearly all patients ultimately acquire resistance to EGFR-TKI treatment. Liver X receptors (LXRs) can regulate tumor growth in various cancer cell lines. The present study indicated that LXR agonist combined with gefitinib weakened Akt-nuclear factor (NF)-κB activation and inhibited the expression levels of apoptosis-related proteins in vitro. By contrast, LXR ligands alone exhibited no significant effect on gefitinib-resistant lung cells. In conclusion, the study provided evidence for the combination treatment of acquired TKI resistance in NSCLC.